These authors contributed equally to this work.
The Bordetella pertussis Bps polysaccharide enhances lung colonization by conferring protection from complement-mediated killing
Article first published online: 13 FEB 2014
© 2014 John Wiley & Sons Ltd
Volume 16, Issue 7, pages 1105–1118, July 2014
How to Cite
Ganguly, T., Johnson, J. B., Kock, N. D., Parks, G. D. and Deora, R. (2014), The Bordetella pertussis Bps polysaccharide enhances lung colonization by conferring protection from complement-mediated killing. Cellular Microbiology, 16: 1105–1118. doi: 10.1111/cmi.12264
- Issue published online: 19 JUN 2014
- Article first published online: 13 FEB 2014
- Accepted manuscript online: 20 JAN 2014 06:02AM EST
- Manuscript Accepted: 6 JAN 2014
- Manuscript Revised: 24 DEC 2013
- Manuscript Received: 2 OCT 2013
- NIH. Grant Number: 1R01AI075081
Bordetella pertussis is a human-restricted Gram-negative bacterial pathogen that causes whooping cough or pertussis. Pertussis is the leading vaccine preventable disease that is resurging in the USA and other parts of the developed world. There is an incomplete understanding of the mechanisms by which B. pertussis evades killing and clearance by the complement system, a first line of host innate immune defence. The present study examined the role of the Bps polysaccharide to resist complement activity in vitro and in the mouse respiratory tract. The isogenic bps mutant strain containing a large non-polar in-frame deletion of the bpsA–D locus was more sensitive to serum and complement mediated killing than the WT strain. As determined by Western blotting, flow cytometry and electron microscopic studies, the heightened sensitivity of the mutant strain was due to enhanced deposition of complement proteins and the formation of membrane attack complex, the end-product of complement activation. Bps was sufficient to confer complement resistance as evidenced by a Bps-expressing Escherichia coli being protected by serum killing. Additionally, Western blotting and flow cytometry assays revealed that Bps inhibited the deposition of complement proteins independent of other B. pertussis factors. The bps mutant strain colonized the lungs of complement-deficient mice at higher levels than that observed in C57Bl/6 mice. These results reveal a previously unknown interaction between Bps and the complement system in controlling B. pertussis colonization of the respiratory tract. These findings also make Bps a potential target for the prevention and therapy of whooping cough.